Evidence for the separation of albumin- and apo A-I-dependent mechanisms of cholesterol efflux from cultured fibroblasts into human plasma.
The role of albumin has been studied in the plasma-mediated efflux of cholesterol from cultured fibroblasts. Immunoaffinity chromatography of plasma on immobilized anti-albumin antibody decreased by 25-50% total efflux catalyzed by plasma. The remainder of the efflux-promoting capacity of plasma was deleted by immunoaffinity chromatography on antibody to apolipoprotein A-I, the major apoprotein of high density lipoprotein. Both components of efflux were saturable with half-saturation at 0.5-1.0% (v/v) plasma. However, the net transport of sterol from cells to medium catalyzed by lecithin:cholesterol acyltransferase, was not reduced by the deletion of the albumin-catalyzed component of efflux. This finding was confirmed with congenitally analbuminemic plasma. These results indicate that efflux to albumin and to high density lipoprotein in plasma represent independent mechanisms; only the latter is coupled to net transport.
D016632:Apolipoprotein A-I; D001053:Apolipoproteins / Q000502:physiology*; D002478:Cells, Cultured; D002784:Cholesterol / Q000097:blood / Q000378:metabolism*; D005347:Fibroblasts / Q000378:metabolism; D006801:Humans; D007223:Infant; D007700:Kinetics; D008075:Lipoproteins, HDL / Q000502:physiology*; D008297:Male; D012709:Serum Albumin / Q000502:physiology*; D012867:Skin / Q000378:metabolism
D016632:Apolipoprotein A-I; D001053:Apolipoproteins; D008075:Lipoproteins, HDL; D012709:Serum Albumin; D002784:Cholesterol